Abstract
We have previously shown a high frequency of allele loss at D6S193 (62%) on chromosomal arm 6q27 in ovarian tumours and mapped the minimal region of allele loss between D6S297 and D6S264 (3 cM). We isolated and mapped a single non-chimaeric YAC (17IA12, 260–280 kb) containing D6S193 and D6S297. A further extended bacterial contig (between D6S264 and D6S149) has been established using PACs and BACs and a transcript map has been established. We have mapped six new markers to the YAC; three of them are ESTs (WI-15078, WI-8751, and TCP10). We have isolated three cDNA clones of EST WI-15078 and one clone contains a complete open reading frame. The sequence shows homology to a new member of the ribonuclease family. The other two clones are splice variants of this new gene. The gene is expressed ubiquitously in normal tissues. It is expressed in 4/8 ovarian cancer cell lines by Northern analysis. The gene encodes for a 40 kDa protein. Direct sequencing of the gene in all the eight ovarian cancer cell lines did not identify any mutations. Clonogenic assays were performed by transfecting the full-length gene in to ovarian cancer cell lines and no suppression of growth was observed.
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Acknowledgements
Dr Iain Goldsmith is acknowledged for synthesis of oligonucleotides, Mr Reginald Boone and Dr Anna Richardson for assistance with sequencing. The FOP clone was obtained from Dr MJ Pebusque. YAC 17IA12 was obtained from Dr J Boyle. Gridded YAC and cDNA libraries were obtained from the MRC HGMP centre. We would like to thank all the members of the chromosome 6 project group at Sanger Centre. The work described in this paper is supported by the Imperial Cancer Research Fund, Association of International Cancer Research, Wellbeing and Human mapping/sequencing at the Sanger Centre is funded by the Wellcome Trust.
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Liu, Y., Emilion, G., Mungall, A. et al. Physical and transcript map of the region between D6S264 and D6S149 on chromosome 6q27, the minimal region of allele loss in sporadic epithelial ovarian cancer. Oncogene 21, 387–399 (2002). https://doi.org/10.1038/sj.onc.1205067
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DOI: https://doi.org/10.1038/sj.onc.1205067